Cardiac Glycoside Plant Poisoning Clinical Presentation
- Author: Raffi Kapitanyan, MD; Chief Editor: Asim Tarabar, MD more...
History
As with all toxic exposures, history should focus on answering the following 6 key questions:
- Who was exposed and are there other victims?
- To what were they exposed?
- When were they exposed?
- Where were they exposed?
- Why were they exposed (unintentional vs intentional)?
- To how much were they exposed (eg, amount, concentration)?
Although acute and chronic plant cardiac glycoside toxicity are treated in similar manners, their noncardiac clinical manifestations differ. In acute toxicity, the following may be present:
- GI symptoms, usually evolve within minutes to hours, are nonspecific, and include nausea, vomiting, and abdominal pain.
- Neurological symptoms often are nonspecific and include weakness and altered mental status (eg, disorientation, confusion, lethargy).
In chronic toxicity, signs and symptoms are insidious, which make diagnose difficult at times. GI symptoms are nonspecific and include anorexia, nausea, vomiting, diarrhea, abdominal pain, and weight loss. Neurological symptoms include confusion, drowsiness, disorientation, delirium, headache, hallucinations, and seizures. Visual disturbances manifest as photophobia, blurry vision, scotomas, decreased visual acuity, and color vision aberrations (eg, chromatopsia, xanthopsia [ie, yellow halos around lights]).
Cardiac symptoms are similar in both acute and chronic toxicity and include palpitations, chest pressure or shortness of breath, lightheadedness, dizziness, and faintness.
Physical
Focus is on cardiovascular, neurologic, and GI systems.
Vital signs
Bradycardia or tachycardia may be seen. In absence of concomitant ingestion, environmental exposure, thyroid disorder, or underlying infection, patient generally is normothermic.
Lungs
Examination findings typically are normal in the absence of preexisting disease, but rales have been reported.
Heart
Bradydysrhythmias or tachydysrhythmias can occur, typically with increased automaticity and depressed conduction. Pulses may be weak, thready, and irregular.
Abdomen
Abdomen is generally soft. Vomiting and diarrhea may be noted. Emesis may contain plant material.
Neurologic
Findings may include an altered level of consciousness, hypotonia, hyporeflexia, dysarthria, ataxia, horizontal nystagmus, and generalized seizures. The patient typically has a nonfocal neurologic examination with pupillary reflexes intact.
Skin
Skin may be pale, diaphoretic, and cool.
Causes
Exposure to plants containing glycosides can occur through ingestion of sap, berries, leaves, blossoms, seeds, or ingestion of teas brewed from plant parts; plant extracts also have been intentionally injected.
Other implicated routes of exposures, perhaps more folkloric than well documented, include drinking lily-of-the-valley vase water, eating food prepared with or stirred by poisonous plant parts, and inhaling smoke from burning plants.
While there are many plant sources of cardiac glycosides, common ones include the following:
- Purple foxglove (Digitalis purpurea)
- Woolly foxglove (Digitalis lanata)
- Ouabain (Strophanthus gratus)
- Lily-of-the-valley (Convallaria majalis)
- Common oleander (Nerium oleander)
- Yellow oleander (Thevetia peruviana)
- Squill or sea onion (Urginea maritima)
Bessen HA. Therapeutic and toxic effects of digitalis: William Withering, 1785. J Emerg Med. 1986;4(3):243-8. [Medline].
Bronstein, AC, Spyker, DA, Cantilena Jr., LR, et al. 2006 annual report of the American Association of Poison Control Centers National Poison Data System. Clinical Toxicology. Dec 2007;45(8):815-917.
Eddleston M, Ariaratnam CA, Sjostrom L, Jayalath S, Rajakanthan K, Rajapakse S. Acute yellow oleander (Thevetia peruviana) poisoning: cardiac arrhythmias, electrolyte disturbances, and serum cardiac glycoside concentrations on presentation to hospital. Heart. Mar 2000;83(3):301-6. [Medline].
Gowda RM, Cohen RA, Khan IA. Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications. Heart. Apr 2003;89(4):e14. [Medline].
Hack JB, Woody JH, Lewis DE, et al. The effect of calcium chloride in treating hyperkalemia due to acute digoxin toxicity in a porcine model. J Toxicol Clin Toxicol. 2004;42(4):337-42. [Medline].
Roberts DM, Buckley NA. Antidotes for acute cardenolide (cardiac glycoside) poisoning. Cochrane Database Syst Rev. Oct 18 2006;CD005490. [Medline].
Bain RJ. Accidental digitalis poisoning due to drinking herbal tea. Br Med J (Clin Res Ed). Jun 1 1985;290(6482):1624. [Medline].
Cheung K, Urech R, Taylor L. Plant cardiac glycosides and digoxin Fab antibody. J Paediatr Child Health. Oct 1991;27(5):312-3. [Medline].
Dickstein ES, Kunkel FW. Foxglove tea poisoning. Am J Med. Jul 1980;69(1):167-9. [Medline].
Eddleston M, Rajapakse S, Rajakanthan, Jayalath S, Sjostrom L, Santharaj W. Anti-digoxin Fab fragments in cardiotoxicity induced by ingestion of yellow oleander: a randomised controlled trial. Lancet. Mar 18 2000;355(9208):967-72. [Medline].
el Bahri L, Djegham M, Makhlouf M. Urginea maritima L (Squill): a poisonous plant of North Africa. Vet Hum Toxicol. Apr 2000;42(2):108-10. [Medline].
Furbee B, Wermuth M. Life-threatening plant poisoning. Crit Care Clin. Oct 1997;13(4):849-88. [Medline].
Goldfrank, Flomenbaum, Lewin, et al. Cardiac glycosides. In: Goldfrank's Toxicologic Emergencies. 7th ed. 2002:724-734.
Rich SA, Libera JM, Locke RJ. Treatment of foxglove extract poisoning with digoxin-specific Fab fragments. Ann Emerg Med. Dec 1993;22(12):1904-7. [Medline].
Plants - cardiac glycosides. In: Rumack BH, ed. Poisondex. 1997:94.
Slifman NR, Obermeyer WR, Aloi BK, Musser SM, Correll WA Jr, Cichowicz SM. Contamination of botanical dietary supplements by Digitalis lanata. N Engl J Med. Sep 17 1998;339(12):806-11. [Medline].
Van Deusen SK, Birkhahn RH, Gaeta TJ. Treatment of hyperkalemia in a patient with unrecognized digitalis toxicity. J Toxicol Clin Toxicol. 2003;41(4):373-6. [Medline].
Print
